转基因小鼠
急性呼吸窘迫综合征
败血症
转基因
生物
发病机制
急性呼吸窘迫
基因
免疫学
遗传学
医学
内科学
肺
标识
DOI:10.1016/j.molimm.2022.10.003
摘要
I read with interest the article authored by Zhang et al. (2020) who examined the role of S100A12 in the pathogenesis of sepsis-induced ARDS (acute respiratory distress syndrome). They used wild-type (WT) mice to measure the expression of S100A12 after induction of sepsis in mice. Based on the fact that S100A12 is not present in the murine genome, the interpretation of the findings could be misleading. Therefore, I discuss the use of S100A12 transgenic mouse models to examine S100A12 expression in mice.
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